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1.
Journal of Zhejiang University. Science. B ; (12): 89-101, 2022.
Article in English | WPRIM | ID: wpr-929042

ABSTRACT

Cancer is the leading cause of death worldwide. Drugs play a pivotal role in cancer treatment, but the complex biological processes of cancer cells seriously limit the efficacy of various anticancer drugs. Autophagy, a self-degradative system that maintains cellular homeostasis, universally operates under normal and stress conditions in cancer cells. The roles of autophagy in cancer treatment are still controversial because both stimulation and inhibition of autophagy have been reported to enhance the effects of anticancer drugs. Thus, the important question arises as to whether we should try to strengthen or suppress autophagy during cancer therapy. Currently, autophagy can be divided into four main forms according to its different functions during cancer treatment: cytoprotective (cell survival), cytotoxic (cell death), cytostatic (growth arrest), and nonprotective (no contribution to cell death or survival). In addition, various cell death modes, such as apoptosis, necrosis, ferroptosis, senescence, and mitotic catastrophe, all contribute to the anticancer effects of drugs. The interaction between autophagy and these cell death modes is complex and can lead to anticancer drugs having different or even completely opposite effects on treatment. Therefore, it is important to understand the underlying contexts in which autophagy inhibition or activation will be beneficial or detrimental. That is, appropriate therapeutic strategies should be adopted in light of the different functions of autophagy. This review provides an overview of recent insights into the evolving relationship between autophagy and cancer treatment.


Subject(s)
Humans , Antineoplastic Agents/therapeutic use , Apoptosis , Autophagy/physiology , Necrosis/drug therapy , Neoplasms/therapy
2.
Journal of China Pharmaceutical University ; (6): 496-502, 2017.
Article in Chinese | WPRIM | ID: wpr-615021

ABSTRACT

The antibacterial activity and mechanism of the antimicrobial peptide mutant Cbf-14-2 against NDM-1 carrying recombinant bacteria (E.coli BL21 (DE3)-NDM-1) was investigated in this study.The minimum inhibitory concentration (MIC),minimum bactericidal concentration (MBC) and killing curves (KCs) in vitro were determined by the broth microdilution method.Mice septicemia model was established by interaperitotoneal injection of E.coli BL21 (DE3)-NDM-1 to evaluate the antibacterial activity of this peptide in vivo.Results showed that Cbf-14-2 exhibited a potent antibacterial activity with MIC of 16 μg/mL and killed almost all recombinant bacteria within 120 min.Meanwhile,it significantly improved the survival rate of infected mice up to 70% with the decreasing of bacterial load in mice lung,liver,spleen and kidney.This powerful clearance ability of Cbf-14-2 against bacteria mainly related to its enhanced membrane penetration ability through neutralizing the negative charges and disrupting the integrity of the bacterial cell membrane.Therefore,Cbf-14-2 is expected to be a potential antimicrobial agent for the treatment of infection induced by multi-drug resistant bacteria,especially for the NDM-1carrying bacteria.

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